Continuity of Care: Treating the Cataract Patient

Cheryl A. Grandinetti, PharmD

Published Online: Tuesday, January 1, 2008

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Dr. Grandinetti is a senior clinical
research pharmacist at the National
Cancer Institute, National Institutes
of Health, Rockville, Maryland. The
views expressed are those of the
author and not those of any government
agency.

The World Health Organization
estimates that 37 million people
are blind, with almost 82% of
them aged 50 years or older.1,2 Cataract
causes almost half of blindness globally
and occurs more frequently in developing
countries.3 Women are at a slightly
greater risk than men, with an estimated
female-to-male ratio of 1.5 to 2.2.

Cloudy or opaque cataracts on the
lens of the eye are generally caused by a
denaturing of crystallins, the major lens
protein.4 In cataracts, less light reaches
the retina, impairing vision and decreasing
quality of life. Three subtypes, defined
by clinical appearance and location, are
nuclear, cortical, and posterior subcapsular
(PSC) cataracts. Each has different symptoms
and risk factors and occurs at different
rates in different populations.1,5-10

The most common cause is aging, but
atopic diseases and their treatments, diabetes,
trauma, and congenital disorders
can cause cataracts, too. Some drugs,
such as those causing photosensitivity,
and radiation therapy are associated
with cataract formation.11 Several studies
have associated long-term corticosteroid
use (at prednisone doses of ≥10-15
mg/day) with PSC formation.12-16 This
association is stronger with oral steroids
than with inhaled steroid use, and children
appear to be particularly at risk.7
Cataracts may progress even after stopping
the corticosteroid. Clinicians should
order comprehensive eye exams more
frequently in individuals with predisposing
risk factors.

Table

At Surgery

Surgery is the only treatment option
and should be considered when the
cataract impairs the patient's ability to
function in daily life.17 Cataract surgery
has a 95% or better success rate in
healthy eyes. It involves removing the
lens and replacing it with an intraocular
lens. During surgery, adequate pupil dilation
must be maintained to remove the
crystalline lens and implant the corrective
intraocular lens without causing
trauma to the iris. Prostaglandin release
can cause surgically induced miosis and
increase the risk of postoperative surgical
complications.

Alpha1 adrenoceptor blockers can
increase the likelihood of surgical complications
by causing the pupil to suddenly
constrict during the operation.5
Discontinuing the drug before surgery
has not yet been evaluated; however,
planned measures, such as iris hooks,
iris dilator rings, or viscoelastic devices,
can minimize the potential complications.18 Topical nonsteroidal anti-inflammatory
drugs (NSAIDs) are often used
to inhibit surgically induced miosis.19

Table

After Surgery

Although postsurgical complications
are infrequent, patients are often started
on topical antibiotic, corticosteroid, and
NSAID drops to prevent complications.9,17

Early diagnosis and treatment of
endophthalmitis, a serious eye infection,
is critical to prevent vision loss. Empiric
therapy is based on the suspected
microorganism most likely encountered
during surgery, from the patient's conjunctiva,
eyelids, or nose. The most common
microorganisms are gram-positive
Staphylococcus aureus and Staphylococcus
epidermidis. Gram-negative infections
with Pseudomonas spp and
Propionbacterium acnes occur less frequently.
The treatment includes intravitreal
injections of vancomycin and ceftazidime
or amikacin (for patients sensitive
to beta lactams). Another treatment
option is broad-spectrum oral fourth generation
fluoroquinolones. The
patients are often treated prophylactically
before surgery with topical povidoneiodine
or topical, subconjunctival, systemic,
or intracameral antibiotics.20,21

Cystoid macular edema (CME), fluid
accumulation in the central retina, is the
most frequent cause of vision loss. It usually
occurs 4 to 6 weeks after surgery,
and symptoms include blurred or declining
central vision and painless retinal
inflammation and swelling. Vision loss is
usually temporary. Clinicians should suspect
CME in any patient with worse-than-expected vision after surgery.19
Most patients experience some postoperative
inflammation. If left untreated,
inflammation may cause discomfort, delay
recovery, decrease vision, and lead to
other complications.22

Combination therapy with a topical
NSAID and/or corticosteroid is indicated
for documented CME and inflammation.
CME treatment starts 1 week before surgery
and continues for at least 4 weeks,
up to several months after surgery. When
treating inflammation, NSAIDs are generally
started 24 hours after surgery and
continued for up to 14 days (Table).
Topical steroids are generally administered
for 2 to 6 weeks after surgery.19,22

Most adverse events following topical
NSAIDs are local, such as burning, stinging,
conjunctivitis, atonic mydriasis, and
local anesthetic effects, as well as pruritus,
erythema, and edema of the bulbar
conjunctiva and lids. Systemic reactions
occur rarely. Increased intraocular pressure
and delayed wound healing are
associated with topical corticosteroids.
NSAIDs are useful alternatives for patients
who develop increased intraocular
pressure while using topical steroids.19